ArticleHelicobacter2012
Helicobacter pylori-associated regulation of forkhead transcription factors FoxO1/3a in human gastric cells.
Article in Helicobacter, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.
- Infiltration to infection: key virulence players of Helicobacter pylori pathogenicity.Infection · 2024Pooled it
- Population, Epidemiological, and Functional Genetics of Gastric Cancer Candidate Genes in Peruvians with Predominant Amerindian Ancestry.Digestive diseases and sciences · 2016Pooled it
- Akt Signaling Pathway Is Activated in the Minor Salivary Glands of Patients with Primary Sjögren's Syndrome.International journal of molecular sciences · 2021Trial
- The Antioxidant and anti-inflammatory Activity of Selenium and Lecithin Combination Against ethanol-induced Gastric Ulcer in mice via Modulating IGF-1/PTEN/Akt/FoxO3a Signaling.Biological trace element research · 2024Article
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Treating chronic atrophic gastritis: identifying sub-population based on real-world TCM electronic medical records.Frontiers in pharmacology · 2024Article
- Molecular mechanisms underlying the action of carcinogens in gastric cancer with a glimpse into targeted therapy.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- From microbiota toward gastro-enteropancreatic neuroendocrine neoplasms: Are we on the highway to hell?Reviews in endocrine & metabolic disorders · 2021Review
- Genetic populations and virulence factors of Helicobacter pylori.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2018Review
- FOXO1: Another avenue for treating digestive malignancy?Seminars in cancer biology · 2018Review
- NLRP6, decreased in gastric cancer, suppresses tumorigenicity of gastric cancer cells.Cancer management and research · 2018Article
- Review
- FOXO responses to Porphyromonas gingivalis in epithelial cells.Cellular microbiology · 2015Article
- Article
- What exists beyond cagA and vacA? Helicobacter pylori genes in gastric diseases.World journal of gastroenterology · 2015Review
- Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways.Cell communication and signaling : CCS · 2015Review
- Helicobacter pylori CagA Suppresses Apoptosis through Activation of AKT in a Nontransformed Epithelial Cell Model of Glandular Acini Formation.BioMed research international · 2015Article
- Helicobacter pylori virulence and cancer pathogenesis.Future oncology (London, England) · 2014Review
- The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis.Cell communication and signaling : CCS · 2013Review
- The Role of Helicobacter pylori Outer Membrane Proteins in Adherence and Pathogenesis.Biology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundInteraction of Helicobacter pylori with gastric mucosa leads to marked cellular and humoral host immunologic responses. The signaling pathways initiated by bacteria-host interaction that result in perturbations in cell structure and function remain unclear. Forkhead transcription factors of class O (FoxO) are implicated in the regulation of apoptosis, cell survival, and pathogenesis. H. pylori infection of gastric epithelial cells induces phosphoinositide-3 kinase (PI3K)-dependent Akt activation and cell survival signaling. We investigated the role of H. pylori-activated PI3K/Akt in the regulation of FoxO1/3a in gastric cells.
methodsImmunoblot, immunoprecipitation, and fluorescence microscopy were used to assess the effect of infection of gastric epithelial cells with wild-type H. pylori and their isogenic cag pathogenicity island (PAI) or oipA mutants on the FoxO1/3a signaling pathways. Interleukin-8 release was determined by enzyme-linked immunosorbent assays.
resultsH. pylori infection resulted in activation of the PI3K p85 subunit and inactivation of FoxO1 and FoxO3a by their phosphorylation and translocation of from the nucleus to the cytoplasm. Inhibition of PI3K or Akt kinase activity reduced FoxO1/3a phosphorylation. Akt, FoxO1, or FoxO3a siRNA reduced H. pylori-induced interleukin-8 production. Infection with oipA mutants reduced PI3K/Akt activation and inhibited FoxO1/3a phosphorylation, whereas infection with cag PAI mutants reduced PI3K/Akt activity but did not inhibit FoxO1/3a activation.
conclusionsFoxO1 and FoxO3a are novel nuclear substrates of H. pylori-induced PI3K/Akt cell survival signaling pathways that partially control interleukin-8 production. OipA-regulated interleukin-8 release through PI3K/Akt is dependent on FoxO1/3a inactivation, whereas cag PAI-mediated interleukin-8 production employs FoxO1/3-independent signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.